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Flashcards in Nerve & Muscle Cells Deck (14):

What is a withdrawal reflex? Outline the sequence of events in the withdrawal reflex. What are the additional important characteristics/What are the effects of a polysynaptic reflex?

1. Withdrawal reflex is
- A polysynaptic reflex in response to painful/nociceptic stimuli
- Acts as survival/protective factor

2. Adequate nociceptive/painful stimuli applied
- Causes flexion response + inhibits extensor response of limb -> Flexion withdrawal from stimulus
- Causes cross extensor response -> Extension of contralateral limb to stabilise body

3. Prolonged/magnified effect where the greater the stimulus, the stronger and longer the reflex response due to
- Impulse arrival at effector at different timings due to interneurons
- Irradiation of impulse up and down the spinal cord
- Recruitment of motor units
- Reverberation of circuit as some interneurons turn back on themselves further prolonging the effect


Please describe the withdrawal reflex. What is meant by the term polysynaptic?

1. Withdrawal reflex is a polysynaptic reflex in response to a painful/nociceptive stimulus with the reflex arc consisting of
- Sensory organ: Nociceptors -> skin, subcutaneous tissue
- Afferent limb: Sensory/pain fibres to dorsal horn of spinal cord
- Central integrator: Polysynaptic connections in spinal cord
- Efferent limb: Motor fibres to effectors
- Effectors: Muscles of ipsi and contralateral limbs

2. Polysynaptic reflex
- One or more interneurons are interposed between afferent and efferent neurons


Describe the sequence of events in contraction of skeletal muscle after the arrival of nerve impulse at motor end plate. Describe the steps in relaxation of skeletal muscle.

1. Contraction of skeletal muscle
- Nerve impulse arrives
- Motor neuron discharges
- Acetylcholine released
- Acetylcholine binds to nicotinic receptors at motor end-plate
- Increases Na + K conductance
- Generates end-plate potential
- Generates action potential which diffuses into T-tubules
- Release of Ca from sarcoplasmic reticulum which diffuses into thin and thick filaments
- Ca binds to troponin C on actin
- Exposes myosin-binding site
- Cross-linkage of myosin and actin
- Power stroke occurs where thin filaments slide on thick filaments producing movements

2. Relaxation of skeletal muscle
- Ca pumped back into sarcoplasmic reticulum
- Ca unbinds from troponin C
- Cessation of linkage between actin and myosin
- Relaxation of smooth muscle


Draw a skeletal muscle action potential.

1. Skeletal muscle action potential
- Phase 1 = Resting membrane potential -90mV, Na + K channels closed
- Phase 2 = Threshold potential -50mV, Na channels start to open
- Phase 3 = Depolarization 30mV, Na channels open
- Phase 4 = Repolarization, Na channels close, K channels open
- Phase 5 = Hyperpolarization, excess K efflux out of cell, K channels start to close
- Phase 6 = Resting membrane potential -90mV
- Action potential duration 5ms


What is the summation of contractions? What are the major differences in types of skeletal muscles?

1. Summation of contractions is the electrical response of a muscle fibre to repeated stimuli
- Contractile mechanism has no refractory period
- If muscle fibre is stimulated before relaxation occurs, it is added on to the already present contraction response
- If this occurs rapidly and repeatedly, the individual responses are fused into one continuous contraction known as tetanus
- Complete tetanus is when there is no relaxation between stimuli
- Incomplete tetanus is when there is incomplete relaxation between stimuli

2. Types of skeletal muscles
A. Type 1 = Slow, white, oxidative
- Maintain posture
- Slow ATPase rate
- Small diameter
- High oxidative capacity
- Moderate glycolytic capacity
- Resistant to fatigue
B. Type 2 = Fast, red, glycolytic
- Produce purposeful movements
- Fast ATPase rate
- Large diameter
- Slow oxidative capacity
- High glycolytic capacity
- Fatigable


Describe the sequence of events in contraction and relaxation of visceral smooth muscle. What factors influence intestinal smooth muscle contraction?

1. Contraction of smooth muscle
- Nerve impulse arrives
- Acetylcholine released which binds to muscarinic receptors
- Increase in Ca influx into cells
- Activates calmodulin-dependent myosin light chain kinase
- Phosphorylates myosin
- Increase myosin ATPase activity causing myosin to bind onto actin
- Contraction occurs

2. Relaxation of smooth muscle cells
- Myosin is dephosphorylated by myosin light chain phosphatase
- Relaxation or sustained contraction due to latch bridge occurs

3. Factors influencing intestinal smooth muscle contraction
- Stretch on visceral -> Increases contraction
- Cold -> Increases contraction
- Acetylcholine -> Increases contraction
- Adrenaline and noradrenaline -> Reduces contraction
- Neural stimulation -> Increase contraction


Describe the neural connections of the visual pathway. Why is the fovea important for visual acuity? What ocular factors influence visual acuity? How is visual acuity measured? What does fractions of VA of 6/24 represent?

1. Neural connections of visual pathway
- Light hits retina -> Optic nerve -> Optic chiasm -> Nasal fibres decussate at optic chiasm to contralateral side -> Optic tract -> Lateral geniculate body -> Occipital lobe (Primary visual cortex)

2. Fovea is centre of macula
- Point of best visual acuity due to
- Highest density of cones

3. Ocular factors influencing visual acuity
- Optical factors -> Cataracts, myopia, hyperopia, astigmatism
- Retinal factors -> Retinopathies (DM, HTN), optic neuritis
- Stimulus factors -> Brightness of stimulus, contrast between stimulus and background

4. Visual acuity is measured using Snellen’s chart at 6 metres

5. Visual acuity of 6/24 represents reduced visual acuity
- Patient is able to read at 6 metres but normal populations are able to read the same at 24 metres


What are the different types of nerve fibres? What classifications are there? What is the clinical relevance to emergency medicine?

1. Nerve fibres can be differentiated by their size and conduction speed
- Large diameter -> Faster conduction -> Proprioception, somatic motor, conscious touch
- Small diameter -> Slower conduction -> Pain, temperature, autonomic functions

2. Classifications
- Gasser classification
+ Aa: Proprioception, somatic motor
+ Ab: Pressure, touch
+ Ag: Muscle spindle
+ Ad: Pain, temperature
+ B: Pre-ganglionic autonomic
+ C dorsal: Pain, temperature
+ C sympathetic: Postganglionic sympathetic

3. Clinical relevance in ED
- Infiltration with local anaesthetic will block pain pathways first and not affect touch, pressure or proprioception


What are upper motor neurons? What clinical features are seen when they are injured? What is clonus? What is the physiological basis of clonus? List the long-term complications of spinal cord injury.

1. Upper motor neurons are corticospinal neurons that innervate spinal motor neurons

2. Clinical features of upper motor neuron
- Initial, paralysis of muscles and flaccidity
- Eventually develop spasticity, hypertonia, hyper-reflexia and upgoing plantars (Babinski reflex)

3. Clonus is
- Repetitive, regular, rhythmic contraction of muscles due to sustained and sudden stretch

4. Clonus is due to
- Loss of descending input to inhibitory neuron
- Loss of inhibition of antagonist
- Resulting in repetitive contraction of ankle flexors and extensors

5. Long term complications of spinal cord injury
- Ulcers
- UTIs due to need for IDC
- Bowel incontinence
- Muscle atrophy
- Hypercalcemia
- Renal calculi
- Thrombosis
- Spinal shock syndrome


What is the function of the reticular activating system? Describe its location and structure

1. Reticular activating system
- Centre within network that regulates respiratory, cardiovascular, endocrine functions
- Sends signal mainly to thalamus
- Increased consciousness, sensory perception, alertness

2. RAS
- Complex polysynaptic network
- Located in mid-ventral portion of medulla and mid-brain
- Converging sensory fibres from long tract and cranial nerves


Describe the components of the stretch reflex. How is it different from the withdrawal reflex? What is an inverse stretch reflex? How do muscle spindles function?

1. Stretch reflex is a monosynaptic reflex consists of
- Sensory organ: Muscle spindle
- Afferent nerve
- Integrator: Monosynpase at motor neuron
- Efferent nerve
- Effector organ: Extrafusal fibres
- Eg: Knee jerk, ankle jerk -> Stretch of muscle spindle causes contraction of muscle

2. Withdrawal reflex is a polysynaptic reflex while stretch reflex is a monosynaptic reflex
- Sensory organ: Nociceptor responding to painful stimuli
- Has afferent and efferent nerves
- Integrator is polysynaptic neurons in the spinal cord
- Efferent nerve stimulates ipsilateral and contralateral limb
- Effector
+ Ipsilateral side: Flexion withdrawal of ipsilateral limb and inhibition of extension
+ Contralateral side: Extension of contralateral limb

3. Inverse stretch reflex
- Prolonged stretch of a muscle causing contracted muscle to suddenly relax
- Sensed by sensory organ (Golgi tendon) -> Afferent fibre -> Integrator (Inhibitory interneuron for inverse stretch) -> Efferent fibre -> Effector

4. Muscle spindles have parallel intrafusal fibres that respond to stretch with different dynamic and static responses


How is heat loss from the body? How is fever produced in the body? How does the body produce heat? What temperature-regulating mechanisms are activated by the cold? What part of the brain controls reflex responses activated by the cold and heat? What mechanisms are activated by heat?

1. Heat loss from body via
- Radiation and conduction (70%)
- Vaporization of sweat (25%)
- Respiration
- Defecation and urination

2. Fever is due to
- Pyrogens, exotoxins, inflammation stimulating monocytes and macrophages -> Release of cytokines (IL-1, bradykinin) -> Acts on hypothalamus -> Local production of prostaglandin -> Rises temperature set point -> Fever

3. Body produces heat via
- Basal metabolic rate
- Food intake
- Muscular activity

4. Temperature-regulating mechanisms activated by cold to increase heat production and reduce heat loss
- Shivering
- Hunger
- Curling up
- Increased voluntary muscle activity
- Cutaneous vasoconstriction
- Horripilation
- Increased adrenaline and noradrenaline release

5. Brain control of temperature
- Heat by anterior hypothalamus
- Cold by posterior hypothalamus

6. Mechanisms activated by heat are
- Sweating
- Cutaneous vasodilation
- Anorexia
- Increased respiration
- Reduced metabolic heat production


Where is thirst regulated? What factors increase thirst? In what situations, may thirst sensation be blunted?

1. Thirst regulated in hypothalamus

2. Factor increasing thirst
- Increase osmotic pressure
- Reduce hydrostatic pressure
- Psychogenic thirst
- Others: Prandial drinking

3. Thirst sensation blurred in
- Hypothalamus damage/impairment
- Altered mental status
- High protein diet -> Protein diuresis


Describe how pain is transmitted from the periphery to the brain. How can acute pain be manipulated? What sites do opioid peptides act on? Describe the characteristics of nerve fibres for fast pain and slow pain. What do you understand by the term referred pain.

1. Pain pathway from periphery to brain
- Sensory organ: Nociceptor -> Naked pain nerve endings
- Afferent nerve: Large, fast, myelinated A-delta fibres and slow, small, unmyelinated C fibres
- Dorsal horn of spinal cord (1st order)
- Lateral spinothalamic tract (2nd order)
- Thalamus (3rd order)
- Cerebral cortex

2. Acute pain can be modulated by
- Gate theory -> Stimulation of large touch/pressure afferent fibre inhibits pain pathway in dorsal horn of spinal cord
- Stress-induced analgesia
- Drugs (opioids)
- High centres interpretation of pain

3. Opioid peptides act on
- Receptors in afferent nerve fibres
- Dorsal horn of spinal cord
- Periaqueductal grey mater of brain

4. Characteristics of fast and slow pain fibres
A. Fast fibres = A-delta fibres
- Myelinated
- Large diameter 2 - 5um
- Fast conduction 12 - 30m/s
- Ends in dorsal horn of spinal cord
- Neurotransmitter is glutamate
B. Slow fibres = C fibres
- Unmyelinated
- Small diameter 0.4 - 0.12um
- Slow conduction 0.2 - 0.5 m/s
- Ends in dorsal horn of spinal cord

5. Referred pain
- Irritation of a visceral organ causing pain in a different somatic area
- Pain that originates from one site and presents at another site different from its origin
- Due to common embryogenic origin or dermatomes